Method for treatment of diseases of the optic tract

ABSTRACT

A method for treatment of diseases of the optic tract resides in a rotating magnetic field, which rotates at a variable angular velocity and its rotation is brought in synchronism with the blood flow pulsation in the internal carotid artery, is applied to the bridge of the nose, to the upper portion of the orbit of both eyes, to the temporal areas, to both of the auriculo-temporal regions, and to the region of a projection of the visual analyzers. 
     A device for treatment of diseases of the optic tract, comprising a housing, accommodating a drive and a main permanent magnet whose axle is connected to the shaft of a drive through an elastic element. Besides, a magnetic brake is accommodated in the housing in the zone of action of the magnetic field.

This application is a continuation of application Ser. No. 341,571,filed Apr. 21, 1989 now abandoned.

FIELD OF THE INVENTION

The invention relates generally to medicine and more specifically to amethod for treatment of diseases of the optic tract and to a device forcarrying said method into effect.

The invention is applicable for treatment of optic tract affectionsunder clinical or outpatient conditions, as well as for treatment ofproctologic and gynecologic diseases, morbid conditions secondary toinjuries, parodontosis, chronic inflammatory diseases of the genitalia,and atrophy of the auditory nerve.

BACKGROUND OF THE INVENTION

Known in the present state of the art is a method for treatment ofneuritis of the optic nerve (SU, A, 927,246) by virtue of an effectproduced by a magnetic field having an intensity of from 200 to 400 Oe.Sources of the magnetic field are arranged at the level of a straightline passing through the external auditory pores, and the area of theoptic nerve is exposed to the effect of the magnetic field for 15minutes, a treatment course consisting of 15 to 20 such 15-minutesessions. Three or four treatment courses are carried out at a one- tothree-month interval.

However, said method is not adequately efficient when used for treatmentof optic tract diseases and suffers from substantial disadvantages.

The method makes use of a permanent magnetic field, which is lessefficient than a variable field and the more so a pulsed one.

A permanent magnetic field involves prolonged treatment sessions andhence longer treatment courses.

The method in question supposes only one area to be acted upon, whereasthe optic tract features a definite extent so that all the areas of theoptic tract, that is, the retina, optic nerve, chiasm, geniculate body,and visual analyzers of the cortex of both cerebral hemispheres, cannotbe exposed to the effect of a magnetic field with the same fieldintensity, i.e., the effect on the other areas of the optic tract ismuch less efficient.

Known in the art is a method for treatment of reticular dystrophy (SU,A, 1,204,211), consisting in exposure of the eye to the effect of apermanent magnetic field, the procedure involving application of amagnet having an area of 5.0 to 7.0 cm² and magnetic induction of 150 to200 mT, with its southseeking pole to the patient's temporal region,whereupon the axis of the magnet is aligned with a horizontal straightline passing through the external angle of the infraorbital margin, atreatment session taking 15 to 20 minutes.

However, the aforesaid method is not adequately effective in treatmentof optic tract diseases, since it makes use of a permanent magneticfield, which is less efficient than a variable or a pulsed field.

Moreover, exposure to the effect of a permanent magnetic field involvesprolonged treatment sessions and courses, while application of acurative action upon only one optic tract element fails to providemagnetic field application to other areas of the optic tract, therebyaffecting the curative effect of said optic tract areas.

Further on, a prolonged period of treatment is concerned with the factthat, whenever both eyes are to be treated, the essence of the proposedmethod allows only one eye to be treated at a time, since simultaneoustreatment of both eyes affects badly the rheo-ophthalmic indices of botheyes, a feature that adds more to the duration of the treatment period.

An applicator for magnetotherapy of the eye (SU, A, 1,139,446) is knownto comprise a body and a magnetic element. The applicator is providedwith a coordinate ring and a number of additional magnetic elements,said magnetic elements having polepieces and are situated in the bodyslots with a possibility of radial and longitudinal travel and rotation,while the body itself is turnable with respect to the coordinate ring.

However, the invention under consideration suffers from somedisadvantages, namely, it is constructionally intended for frontalarrangement on the anterior eye portion and cannot be applied to otherocular portions wanting magnetic therapy, thereby being ineffective fortreatment of diseases of the entire optic tract. Besides, the presentdevice fails to provide synchronism of the magnetic field effect withthe blood flow pulsation in the internal carotid artery, which affectsadversely the efficacy of treatment.

One prior-art magnetotherapy device (DE, A, 1,3221544) is known tocomprise a housing accommodating a permanent magnet and a drive whoseshaft is associated with the axle of the permanent magnet.

The operating principle of the known device is based on the fact that arotating magnetic field is established round a rotary permanent magnet,which magnetic field is used to produce a curative effect onto variouspathologic areas. A characteristic feature of the aforesaid known deviceis the fact that the permanent magnet rotates uniformly and its rotationdevelops a sinusoidally variable space magnetic field, which prolongsthe treatment period and affects the curative effect.

The device fails to provide substantially intense induced electricfields when bringing permanent magnet rotation in synchronism with bloodflow pulsation in the internal carotid artery, since to establishhigh-intensity electric fields requires very high values of magneticfield induction (of the order of 1 T), which is practically unattainablein the device under consideration.

The disadvantages stated hereinbefore are fraught with untowards sideeffects, such as headache, abnormally intraocular pressure, which alsoaffects the efficacy of treatment of the optic tract diseases.

SUMMARY OF THE INVENTION

It is an object of the invention to enhance the visual function.

It is another object of the invention to enhance the efficacy oftreatment.

It is a further object of the invention to curtail the treatment time.

These objects are accomplished due to the fact that in a method fortreatment of diseases of the optic tract, comprises exposing it to theeffect of a magnetic field, according to the invention, the magneticfield is applied to the bridge of the nose, the upper portion of theorbit of both eyes with the eyelids closed, the temporal areas close tothe external orbital margin of both eyes, to both of theauriculo-temporal regions at the level of a projection of the opticdecussation, and to the region of a projection of the visual analyzerson the occipital protuberances; when applied to said regions themagnetic field is rotated at a variable angular velocity and itsrotation is brought in synchronism with the blood flow pulsation in theinternal carotid artery.

It is also expedient that a maximum magnetic field induction in theproposed method be from 0.1 to 0.25 T.

It is also expedient that the effect of a rotating magnetic field beapplied to each of the aforesaid regions for 1 to 5 minutes.

These objects are accomplished also due to the fact that a device fortreatment of diseases of the optic tract, comprising a housing whichaccommodates a drive and at least one main permanent magnet whose axleis connected to the drive shaft, according to the invention, is providedwith a magnetic brake accommodated in the housing in the area of themagnetic field effect, while the axle of the permanent magnet isconnected to the drive shaft through an elastic element.

It is also expedient that the magnetic brake of the device proposedherein be made as at least one ferromagnetic rod.

It is also favourable that the magnetic brake be made as at least onepermanent magnet.

It is also expedient that the device be provided with a shield having awindow and arranged round the permanent magnet, said shield being madeof a high-conductance material.

Thus, practical application of the aforedescribed method for treatmentof diseases of the optic tract and the device for carrying said methodinto effect makes it possible to enhance visual functions from two tofifteen times, depending on etiology of a disease, as for acuity ofvision, to increase efficacy of treatment and to cut down the treatmentperiod to 15 days, i.e., one treatment cycle consisting of 15magnetotherapy sessions.

BRIEF DESCRIPTION OF THE DRAWINGS

In what follows the invention is illustrated by specific exemplaryembodiments thereof with reference to the accompanying drawings,wherein:

FIGS. 1 through 3 show areas on human head which are exposed to theeffect of a rotating magnetic field, according to the invention;

FIG. 4 is a general sectional view of a device for treatment of diseasesof the optic tract, according to the invention;

FIG. 5 is a fragmentary sectional view of a device for treatment ofdiseases of the optic tract, incorporating an elastic element made as aflat spiral spring;

FIG. 6 is a section taken along the line VI--VI in FIG. 5;

FIG. 7 is a fragmentary sectional view of a device for treatment ofdiseases of the optic tract, incorporating an elastic element made as alath spring;

FIG. 8 is a section taken along the line VIII--VIII in FIG. 7;

FIG. 9 is a section taken along the line IX--IX in FIG. 4;

FIG. 10 is a general view of a device for treatment of diseases of theoptic tract, according to the invention;

FIG. 11 a general sectional view of an alternative embodiment of thedevice of FIG. 10, according to the invention; and

FIG. 12 is a section taken along the line XII--XII in FIG. 11.

DETAILED DESCRIPTION OF THE INVENTION

The method for treatment of diseases of the optic tract consists in thata magnetic field rotating at a variable angular velocity, is applied toa region 1 (FIGS. 1, 2) of the bridge of the nose, to an upper portionof the orbit of both eyes (with the eyelids closed), to the temporalareas close to an external orbital margin 3 of both eyes, to bothauriculo-temporal areas 4 at the level of a projection of the opticdecussation, and to the region of a projection of visual analyzers onoccipital protuberances (FIG. 3).

Rotation of the magnetic field is brought in synchronism with the bloodflow pulsation in the internal carotid artery, and a maximum magneticfield induction is within 0.1 and 0.25 T.

As it has been demonstrated by clinical practice the sequence ofconduction of stimulation of said areas does not matter. Consideredbelow is one of the variants of the sequence of stimulation of saidareas.

Prior to conducting a treatment procedure the housing of the device fortreatment of diseases of the optic tract is disinfected with ethylalcohol at the spot where the permanent magnet is located. Then therotating magnetic field is synchronized, as for the rotation frequency,with the blood flow pulsation in the internal carotid artery byselecting the rotation frequency of the main permanent magnet equal tothe carotid pulsation rate, using conventional methods. Thereafter thedevice for treatment of diseases of the optic tract is so positionedthat the main permanent magnet be placed closely first on the upperportion 2 (FIGS. 1, 2) of the orbit of one eye, then of the other eye,the eyelids being closed, while exposure time of each of said areas tothe effect of the rotating magnetic field ranges from 1 to 5 minutes.Next the main permanent magnet is placed in the temporal region close tothe external orbital margin of both eyes in succession, the holding timebeing from 1 to 5 minutes for each of the areas. Thereupon the device isdisplaced into the auriculo-temporal area 4 at the level of a projectionof the optic decussation and the permanent magnet put in said area firston one side of the head, then on the other side, the application time ofthe rotating magnetic field being 1 to 5 minutes. Then exposed to theeffect of the rotating magnetic field in a similar way are the areas ofprojection of the visual analyzers on the occipital protuberances 5(FIG. 3) by putting the main permanent magnet of the device on saidareas in succession, the exposure time ranging from 1 to 5 minutes. Thetreatment session terminates in applying the effect of the rotatingmagnetic field to the region 1 of the bridge of the nose (FIGS. 1, 2) byplacing thereon the main permanent magnet of the device, the exposuretime being within 1 and 5 minutes. It should be noticed that theexposure time for each of said areas is individual for every patient.

It is worth noting that individual selection of the exposure time of arotating magnetic field in each of the areas to be treated is determinedby the onset of some disagreeable sensations, such as headache and asense of pressure in the area of the eyeball. The exposure time is to beso varied that such untowards side effects do not occur.

A rotating magnetic field is featured by such parameters as theinduction value and the field intensity vector, i.e., the direction of amagnetic field.

Rotation of a magnetic field results in that the magnetic fieldinduction value at a given point in space or on the area being treated,passes twice through the whole range of magnitudes from the maximum tothe minimum per its complete revolution, with the axis of rotation ofthe main permanent magnet or magnets building up the magnetic field,remaining stationary. The field intensity vector, i.e., the direction ofa line of force of the magnetic field, performs also a completerevolution per field revolution. Thus, both the induction value and thedirection of the magnetic field vary in the area of the fieldapplication during rotation of the main permanent magnet.

As is known from electrodynamics, variation of a magnetic flux (i.e.,magnetic field induction) with time induces an electric field in thearea when said variation takes place, said electric field enveloping thevariable magnetic flux. In this case the value of intensity of thethus-induced electric field depends on the rate of variation of themagnetic flux, i.e., it depends on the maximum and minimum values of themagnetic field induction in the area involved and on the time of saidmagnetic flux variation. This means that the higher the maximuminduction value and the shorter the time of its variation down to theminimum value, or vice versa, the higher the value of intensity of theelectric field induced. When interacting with ions in the vessels,axons, neurons, and other cells or in the intercellular space, aninduced electric field results in arising of induced currents, i.e., intransfer of ions along the electric field lines of force, the rate ofion transfer being in direct proportion with the electric fieldintensity. It is common knowledge that such currents provide for atherapeutic action due to their effect on cell metabolism. Besides, themagnetic field itself is capable of producing a therapeutic effect, thusenlarging vascular lumen, reducing blood coagulability, enhancing tissueoxigenation, abating inflammatory processes, accelerating resolution ofhematomas, and so on.

The results of the work done, clinical experiments and estimationsdemonstrate that a maximum magnetic field induction below 0.1 T fails toprovide a stable therapeutic effect, nor can it give an adequatetreatment efficacy and cut down the treatment time.

A maximum magnetic field induction in excess of 0.25 T, whenever theexposure time in the aforesaid areas is to be cut down, is notpracticable since it involves more side effects.

Besides, it is due to sluggishness of setting a new level of dynamicmetabolic equilibrium in the course of magnetic field application that areduced exposure time restricts a possibility of attaining a positivetherapeutic effect. Thus, application or magnetic fields having theirinduction above 0.25 T is undesirable.

It is due to sluggishness of setting a new level of dynamic metabolicequilibrium in the aforesaid areas in the course of their exposure tothe effect of a rotating magnetic field that the exposure time of saidareas shorter than 1 minute is inefficient and prolongs the treatmentcourse, whereas the exposure time longer than 5 minutes results in theonset of untoward side effects, such as headache, abnormally highintraocular pressure, conjunctivitis, and so on, since permanent andvariable magnetic fields, as well as an electric field induced by thelatter magnetic field and the respective induced currents must not beapplied for a prolonged period of time because of their modifying effectproduced on tissue metabolism.

Rotation of a magnetic field at a variable angular velocity andsynchronization of its rotation with blood flow pulsation in theinternal carotid artery provide for enhanced visual functions, add tothe efficacy of treatment of the optic tract and cut down the treatmentperiod.

The device for carrying the aforesaid method into effect incorporates ahousing 6 (FIG. 4), wherein there are accommodated a main permanentmagnet 7 having an axle 8, and a drive 9 whose shaft 10 is connected tothe axle 8 through an elastic element 11, which may be shaped as a coilspring, flat spiral spring (FIGS. 5, 6) or lath spring (FIGS. 7, 8). Thehousing 6 (FIG. 4) accommodates also a magnetic brake 12, which islocated in the effective area of the magnetic field and is shaped as twoferromagnetic rods 13 (FIG. 9).

The device for treatment of diseases of the optic tract comprises also ashield 14 (FIG. 10) having a window 15 and arranged around the mainpermanent magnet 7 (FIG. 4) in the magnetic field effective area, saidshield being made of a high-conductance material.

Now let us consider an embodiment of the device for treatment ofdiseases of the optic tract as presented in FIG. 11. The main permanentmagnet 7 of the device is composed of two magnets 16 and 17 secured withtheir opposite poles on a faceplate 18 made of, e.g., a ferromagneticmaterial. The magnetic brake 12 is built up of two permanent magnets 19,20 accommodated in the housing 6 under the faceplate 18 so that theirpoles are oriented oppositely with respect to the faceplate 18. Theelastic element 11 is shaped as a flat spiral spring. FIG. 12illustrates the position of the window 15 of the shield 14.

The device for treatment of diseases of the optic tract as shown in FIG.4 functions as follows.

The ferromagnetic rods 13 of the magnetic brake 12 provide for strictorientation of the poles of the main permanent magnet 7 with respect tothe housing 6. Once the shaft 10 of the drive 9 has started rotating theelastic element 11, viz., the spring begins twisting (i.e., to be woundon), this being due to the fact that the ferromagnetic rods 13 of themagnetic brake 12 keep the main permanent magnet 7 fixed stationary, soto say `enslaved`. The elastic element 11, i.e., the spring is beingwound on until the torque on the axle 8 of the main permanent magnet 7gets equal to the torque developed due to magnetic adherence of the mainpermanent magnet 7 to the ferromagnetic rods 13. Once the torque of thewound-up spring (the elastic element 11) has become equal to thatdeveloped by magnetic adherence of the main permanent magnet 7 to theferromagnetic rods 13, with the shaft 10 of the drive 9 rotating, thereoccurs, so to say, `failure` of the magnetic brake 12, i.e., the mainpermanent magnet 7 starts rotating.

As soon as the force applied to the axle 8 of the main permanent magnet7 by the wound-up spring becomes equal to the force of magneticadherence of the main permanent magnet 7 to the ferromagnetic rods 13the angular velocity of rotation of the main permanent magnet 7 getsequal to zero. With the shaft 10 of the drive 9 rotating and the springin the wound-up state the main permanent magnet 7 starts rotating. Asthe angle of rotation of the main permanent magnet 7 increases the forceof magnetic adherence of the latter to the ferromagnetic rods 13 dropsdue to a longer distance therebetween, with the result that the angularvelocity of rotation of the main permanent magnet 7 begins to increase.Once the axle 8 of the main permanent magnet 7 has revolved through 90degrees the forces of magnetic adherence of the opposite poles of themain permanent magnet 7 to the ferromagnetic rods 13 get equal butoppositely directed, while a total force of magnetic adherence becomesequal to zero. As soon as the axle 8 of the main permanent magnet 7rotates through an angle greater than 90 degrees, the force of magneticadherence of its poles to the ferromagnetic rods 13 becomes an analogueof a couple of forces, since its direction coincides with the sense ofrotation of the magnet 7.

Once the angular velocities of the shaft 10 of the drive 9 and of theaxle 8 of the main permanent magnet 7 have equalized, the forces ofmagnetic adherence of the poles of the main permanent magnet 7 to theferromagnetic rods 13, as well as the force of the unwinding spring getequal, while the angular velocity of the axle 8 of the main permanentmagnet 7 starts rising rapidly. At the instant when the angle ofrotation becomes equal to 180 degrees the force of magnetic adherence ofthe poles of the main permanent magnet 7 reaches its maximum value andacceleration of magnetic field rotation becomes also maximum. As aresult, the angular velocity of rotation of the axle 8 of the mainpermanent magnet 7 and hence that of the magnetic field reaches amaximum. In this case the angular velocity of rotation of the shaft 10of the drive 9 proves to be below the angular velocity of rotation ofthe axle 8 of the main permanent magnet 7, while the degree ofwinding-on of the spring decreases.

Once the axle 8 of the main permanent magnet 7 has revolved through anangle exceeding 180 degrees, its angular velocity of rotation startsdecreasing. This is explained by the fact that the force of magneticadherence of the poles of the main permanent magnet 7 to theferromagnetic rods 13 has reached its maximum value, the spring isunwound completely, the angular velocity of rotation of the shaft 10 ofthe drive 9 is below that of the axle 8 of the main permanent magnet 7so that the kinetic energy of rotation stored by the main permanentmagnet 7 is the only principal factor of rotation. As soon theinteraction of the poles of the main permanent magnet 7 dampens out itsrotary inertia, the angular velocity goes to zero, whereas the force ofmagnetic adherence of the main permanent magnet 7 urges it to reversethe sense of its rotation. As a result, a few rotary oscillations of themain permanent magnet 7 occur about a point corresponding to an angle of180 degrees, which oscillations will continue until unidirectionalrotation of the shaft 10 of the drive 9 makes the spring to wind up soas its force of tension becomes equal to the forces of magneticadherence of the polses of the main permanent magnet 7 to theferromagnetic rods 13, whereupon the whole process of rotation of thepermanent magnet 7 will be repeated.

In an embodiment of the device as shown in FIG. 11 used as the magneticbrake 12 are the permanent magnets 19 and 20, which are arrangeddiametrically opposite with respect to the axle 8 of rotation of themain permanent magnet 7 and are oriented with their opposite polesrelative to the faceplate 18, the latter being made of, e.g., aferromagnetic material.

Since magnetic adherence takes place of the permanent magnets 19 and 20to the faceplate 18 similar to that described above, characteristicfeatures of rotation of the main permanent magnet 7 (15, 16) on thefaceplate 18 are similar to those described with reference to theembodiment considered hereinbefore.

Characteristic features of the permanent magnet rotation are somewhatmodified in the case where the faceplate 18 is made of anonferromagnetic material.

In this case use of the magnets 19, 20 oriented with their like polesrelative to the faceplate 18 fails to provide the desired effect ofincreased angular velocity of the main permanent magnet 7, whichprecludes the full accomplishment of the object of the invention. Thisis accounted for by the fact that at any angle of rotation of the mainpermanent magnet 7, its interaction with the permanent magnets 19, 20develops forces that are equal in magnitude but directed oppositely. Inaddition, the relative position of the main permanent magnet 7 and thehousing 6 is not fixed.

Whenever the permanent magnets 19 and 20 are oriented with their unlikepoles with respect to the faceplate 18, there occurs a well-definedposition of the main permanent magnet 7 with respect to the housing 6.However, having once rotated through 90 degrees the main permanentmagnet 7 (16, 17) starts interacting with the permanent magnets 19, 20by virtue of mutual repulsion, i.e., deceleration of rotation of themain permanent magnet 7 (16, 17).

This results in that the angular velocity of rotation of the mainpermanent magnet 7 (16, 17) passes through its minimum with an angle ofrotation equal to 180 degrees. Further velocity rising process occurssimilarly to the embodiment of the device shown in FIG. 4. Thus, in theherein-considered embodiment of the device the angular velocity ofrotation of the main permanent magnet 7 (16, 17) passes through itsmaxima at an angle of 90 degrees and through its minimum at an angle of180 degrees during rotation of the main permanent magnet 7 (16, 17)through an angle of 180 degrees, whereupon said angular velocity startsincreasing, which has been the case with the embodiment of the devicepresented in FIG. 4.

In an embodiment of the device making use of either of the permanentmagnets 19 or 20 oriented with either of its poles with respect to thefaceplate 18, a well-defined fixing of the main permanent magnet 7 (16,17) with respect to the housing 6 is attained, as well as the samemachanism and characteristic features of its rotation as in the case ofthe ferromagnetic faceplate 18.

Thus, a variable angular velocity of rotation of the main permanentmagnet 7 (16, 17) may be attained, in the case of high accelerationvalues, in all cases save an embodiment involving similar orientation ofthe poles of the permanent magnets 19, 20 with respect to the faceplate18 made of a nonferromagnetic material.

The device for treatment of disease of the optic tract is so positionedin each of the areas 1 through 5 to be treated (FIGS. 1 through 3) thatthe main permanent magnet 7 (16, 17) would rotate over said area at anangular velocity varying within a maximum possible range. In this case,with a view to reducing the magnetic field leakage flux the window 15(FIGS. 10, 12) of the shield 14 is located over the area to be exposedto the effect of the magnetic field.

Thus, the embodiments of the device described above provide for magneticfield rotation at a variable angular velocity and hence its change asfor amplitude and direction, which affords, in combination with themethod disclosed herein, enhancing of the visual functions, higherefficacy of treatment and curtailed treatment period.

The proposed method for treatment of diseases of the optic tract and thedevice for carrying said method into effect are illustrated hereinbelowby the following exemplary clinical case histories.

EXAMPLE 1

Female patient who had sustained myelopolyradiculoneuritis, noticedaffected visual acuity in both eyes. Retrohulbar neuritis was diagnosed.After conservative treatment visual acuity in OD remained equal to 0.5,in OS, 0.3 to 0.4. Fields of colour vision narrowed by 20 degrees.According to automatic perimetry findings, reduced light sensitivity inOD (relative narrowing of the visual field to 30 degrees from thefixation point), narrowed visual field in OS on the nasal side, multiplerelative scotomata in the inferonasal portions of the visual field.According to the evidence of electrophysiological examinations, moderatechanges in the inner layer of the retina and in the optic nerve.

On examination of the fundus oculi--the optic disk pallid on thetemporal side, the arteries narrowed and tortuous. No changes in themacular zone. The patient was given 15 one-minute sessions of magneticstimulation with a magnetic field having an induction of 0.1 T. As aresult, visual acuity in OD increased to 0.6, that in OS, to 0.6. Fieldsof colour vision extended by 10 degrees. According to the evidence ofautomatic perimetry relative scotomata disappeared from the visualfield, the peripheral borders extended by 10 degrees. According to thefindings of electrophysiological examination the inner layers of theretina in a normal state, slight changes in the optic nerve. Thefollow-up period--10 months.

EXAMPLE 2

Female patient noted visual impairment from June, 1986. Maculodystrophyin OD was diagnosed. Visual acuity in OD 0.3+1.0 d-0.5. Electricalsensitivity `threshold` equal to 100 μA gave evidence of moderatechanges in the inner layers of the retina. The evidence availabletestified to exudative dysfunction of the pigmented epithelium and ofthe photoreceptors. The visual field narrowed concentrically by 30degrees. According to the findings of automatic perimetry there werenoted multiple paracentral scotomata and narrowed peripheral borders by30 degrees.

The patient was examined by a neuropathologist in order to detect thecause of retinal dystrophy. The examination findings: vegetovasculardystonia against a background of osteochondrosis, angiospasm of thecerebral vessels accompanied by hypertensive disease and metabolicpolyarthritis in the course of involution.

Ocular fundus evidence--the optic disk coloured light pinkish, itsborders clear-out, the arteries narrowed and tortuous. Some dystrophicchanges in the retina (of the cystose type) at the periphery and in thecentral zone. The patient was subjected to 15 two-minute sessions ofmagnetic stimulation with a magnetic field having an induction of 0.1 T.The patient tolerated the treatment course well. Headache that hadtroubled the patient earlier disappeared in the course of treatment.Visual acuity in OD increased to 0.8. According to the evidence ofautomatic perimetry the borders of the visual field normalized. Theelectrical sensitivity `threshold` dropped down to 70 μA, whichevidenced slight changes in the inner layers of the retina.

EXAMPLE 3

Male patient had detected drastic visual impairment in OD a year beforeresorting to a clinic. Visual impairment resulted from circulatorydisturbance in the vessels supplying the optic nerve. No improvement inthe patient's sight ensued from conservative treatment performed. Visualacuity 0.02 (ex) in OD, 0.2+1.0 d=0.6 in OS. The visual field in OSnarrowed concentrically to 10 degrees, no visual field in OD on thenasal side, while on the temporal side it narrowed to 30°. According tothe findings of electrophysiological examinations bad changes in theinner layers of the retina and in the optic nerve.

According to the evidence of computerized tomography the diameter of theright and left optic nerve 4.3 mm, density of the right nerve 21.3Nunits, that of the left nerve, 47N units.

Ocular fundus in OD--the optic disk pallid, its borders clear-cut, thearteries narrowed and tortuous.

Ocular fundus in OS--the optic nerve disk coloured white, its bordersclear-cut, slight parapapillar edema. The arteries narrowed andtortuous, the veins moderately dilated.

The patient underwent 15 5-minute sessions of magnetic stimulation witha magnetic field having an induction of 0.1 T. After the treatment thevisual acuity in OD increased to 0.3+2.0d=0.8, that in OS, to0.4+2.0d=1.0.

The borders of the visual fields extended by 25 degrees. According tothe evidence of electrophysiological examinations, moderate changes inthe inner layers of the retina and in the optic nerve. The follow-upperiod--one year. Visual acuity remains unaffected, the borders of thevisual field has narrowed by 5 degrees.

EXAMPLE 4

Male patient had noticed drastic visual impairment in OS six monthbefore resorting to the clinic. Ischemic neuroretinopathy was diagnosed.The patient was treated conservatively without any positive effect.

Visual acuity in OS, 0.01, unamenable to correction, that of OD0.3+2.5d=0.4.

The visual field of the OS narrowed concentrically to 35 degrees, thatof OD remained unaffected.

Electrophysiological examinations detected considerably changes in theinner layers of the retina and in the optic nerve of OS and moderatechanges in the inner layers of the retina and in the optic nerve of OD.

Occular fundus: OS--the optic disk edematous, its borders blurred andundeterminable, polymorphic hemorrhages along the run of the inferiorvascular bundle and the anteromacular artery, the macular regionunaffected; OD--the optic disk light pinkish, its borders clear-cut,sporadic dystrophic foci in the macular zone.

The patient was given 15 one-minute sessions of magnetic stimulationwith a magnetic field having an induction of 0.2 T in each area. Aftertreatment the visual acuity in OS increased to 0.1+3.0d=0.6, that of OD,to 0.6. The visual field of OS extended by 20 degrees.

Electrophysiological examinations demonstrated an improved state of theinner layers of the retina and of the optic nerve; the electricalsensitivity `threshold` in OD 40, that in OS, 90; electrical lability inOD 40, in OS, 38.

The ocular fundus of OS exhibited lower amount of hemorrhages, no recenthemorrhages were noted.

The follow-up period--6 months, the results of treatment stable.

EXAMPLE 5

Male patient had noticed drastic visual impairment in OD 1.5 yearsbefore resorting to medical aid. Visual acuity in OS dropped graduallyfor 1.5 years. The patient's anamnesis included diabetes mellitus.

On applying to an ophthalmologist there were diagnosed circulatorydisturbance in the vessels supplying the right optic nerve, as well asangiosclerosis and maculodystrophy in OS.

Visual acuity in OD 0.01, unamenable to correction, that of in OS,0.1+1.5d cyl-1.5d=0.2. The visual field in OD absent on the temporalside, a relative central scotoma revealed in the visual field of OS, aswell as concentric narrowing of the borders on the nasal side by 10degrees. The field of colour vision narrowed by 20 degrees in OS, whilethe visual field for red and blue colours in OD narrowed by 20 degrees;no visual field for green colour whatever.

According to the findings of electrophysiological examinations neitherthe electrical sensitivity `threshold` nor electrical lability wasdeterminable in OD; moderate changes in the retina and optic nerve weredetected in OS. Computer tomography revealed some atrophic changes inthe optic nerves of both eyes. Angiosclerosis accompanied by calcinosisin the vascular channel of the internal carotid arteries and of theopthalmic arteries. Age-dependent hydrocephalus. Ultrasonicdopplergraphy revealed a reduced blood supply of the brain and eye, andatherosclerosis-based stenotic processes.

The patient was subjected to 10 2-minute sessions of magneticstimulation with a magnetic field having an induction of 0.2 T, appliedto each area to be treated. Posttreatment visual acuity in OD increasedto 0.3, that of OS, to 1.0. The visual fields in both eyes extended by20 degrees, relative scotomata disappeared from the visual field of OD.The borders of the field of colour vision extended by 10 degrees.

The follow-up period--one year. The treatment results stable.

EXAMPLE 6

Male patient sustained a traumatic lesion of his right eye in 1982.Visual acuity reduced to 0.4. The patient was given conservativetreatment courses which proved to be futile.

The peripheral borders of the visual field remained unaffected. Thevisual fields for red and green colours narrowed to 10 degrees, whilethat for blue colour was absent altogether. Computerized perimetryrevealed some reduction of foveal light sensitivity to 34 db. Almostcomplete loss of the lower half of the visual field, with the centralzone remaining relatively unaffected. Electrophysiological examinationsdetected moderate changes in the functions of the outer layers of theretina; electroretinogram enlarged, an indirect symptom of optic nervepathology.

Ultrasonic dopplerography revealed blood supply of OD reduced to 1 ml/s.Computerized tomography found nonuniform attenuation of the right opticnerve, at some places down to 2.0 mm, its density dropped down to 20Nunits. Moderate induration of the internal carotid arteries at the levelof the clinoid plate; the left optic nerve of normal thickness anddensity.

The patient was given 15 5-minute sessions of magnetic stimulation witha magnetic field having an induction of 0.2 T. Visual acuity in ODrestored to 0.7.

Computerized perimetry demonstrated that foveal sensitivity remained aslow as 32 db, and the lower border of the visual field diminished downto 20°. Dopplerography revealed an improved blood supply of OD.Electroretinogram displayed moderate changes in the central area of theretina.

The follow-up period--6 months. The dynamics remained stable.

EXAMPLE 7

Male patient was given the diagnosis of amblyopia of OD. The visualacuity of the eye had been affected since the age of two years.

Visual acuity in OD--0.3, that in OS--1.0. According to evidenceobtained by means of a dioptron, hypermetropia of +1.0 was detected inOD. No changes in the visual field were found, nor were any changesdetected by electrophysiological examinations.

Computerized perimetry revealed reduced light sensitivity to 28 db, anenlarged blind spot and the presence of relative and absolute scotomata,predominantly on the nasal side.

The patient was given 15 one-minute sessions of magnetic stimulationwith a magnetic field having an induction of 0.25 T. Posttreatmentvisual acuity in OD increased to 1.0. Findings of computerized perimetryand electrophysiological examinations revealed no changes.

The follow-up period--10 months. Visual acuity remained invariably high.

EXAMPLE 8

Male patient had the visual acuity of his right eye affected sincechildhood.

The patient was sent for advice with the diagnosis of convergent squint,mild-degree hypermetropia, amblyopia.

Visual acuity in OD--0.03+1.5d=0.05-0.1, that of OS, 1.0. Ocular fundus:OD--manifested destruction of the pigmented epithelium, three smallwhite foci with clear-cut borders over the foveal region.

Electrophysiological examinations found bad dysfunction of the outerlayers of the retina. Visual fields free from pathology.

The patient was subjected to 15 2-minute sessions of magneticstimulation with a magnetic field having an induction of 0.25 T. As aresult of the treatment performed visual acuity in OD increased to 0.4.Electrophysiological examinations and examination of the visual fieldrevealed no changes.

The follow-up period--6 months.

High visual acuity persisted.

EXAMPLE 9

Female patient applied to an opthalmologist with the diagnosis ofpartial atrophy of the optic nerve in both eyes secondary toarachnoiditis sustained a year before.

Visual acuity: OD--0.6; OS--0.5, unamenable to correction.

Electrophysiological examinations detected drastic changes in the innerlayers of the retina and in the optic nerve. A complex ultrasonicexamination was performed, dopplerography revealed considerablereduction of hemodynamics in the optic nerve of both eyes. The fields ofcolour vision narrowed to 5 degrees in both eyes, peripheral borders ofthe visual field narrowed to 20 degrees in OD and to 40 degrees in OS.

Computerized tomography revealed a reduced diameter of both optic nervesto 2.8 mm with substantial changes in their density. Consolidated tissuewas revealed in a projection of the right internal carotid artery. Thebasal cisterns dilated due to moderate cerebral atrophy. The patient wasgiven 15 5-minute sessions of magnetic stimulation with a magnetic fieldhaving an induction of 0.25 T applied to each area to be treated.

Posttreatment visual acuity increased to 0.7. The borders of theperipheral visual field extended by 20 degrees, those of the field ofcolour vision, by 10 degrees.

Ultrasonic dopplerography found an improved blood supply of the opticnerve, though its level remained abnormally low.

The dynamic follow-up observation for a 7-month period demonstratedvisual acuity remaining adequately high.

EXAMPLE 10

Female patient was given the diagnosis of partial atrophy of the opticnerve in both eyes. Six months before drastic impairment of visualacuity in OD was noticed, secondary to a hypertensive crisis.

Visual acuity: OD--0.2, OS--0.9.

The ocular fundus exhibited paling of the optic disk on both sides, andangiosclerosis.

Computerized perimetry noted narrowed visual field in the upperportions, largely in OD, relative scotomata in the nasal portion of thevisual fields--symptoms of central-genesis dysfunction of the opticnerves. Computerized tomography revealed consolidated tissues, morepronounced in OD, where petrificates were observed.

The patient was subjected to 10 4-minute sessions of magneticstimulation with a magnetic field having an induction of 0.1 T. As aresult, visual acuity in OD increased to 0.4, that in OS, to 1.0.Computerized perimetry revealed considerable positive dynamics.Electrophysiological examinations detected slightly reduced electricallability (down to 38) in OD.

EXAMPLE 11

Female patient was given the diagnosis of partial atrophy of the leftoptic nerve secondary to arachnoiditis sustained earlier.

Visual acuity: OD--1.0, OS--0.7 to 0.8.

The ocular fundus displayed paling of the optic disk on the temporalside in both eyes.

Electrophysiological examinations revealed moderate changes in the innerlayers of the retina and in the optic nerve. Computerized perimetryfound sporadic scotomata along the periphery of the visual field in ODand scotomata in the nasal half of the visual field and along thevertical meridian in OS. Computerized tomograph detected moderatehydrocephalus, multiple sclerosis in the remission stage, partialatrophy of the optic nerve in both eyes.

The patient was subjected to 15 3-minute sessions of magneticstimulation with a magnetic field having an induction of 0.1 T.Posttreatment visual acuity 1.0 in both eyes. Computerized perimetrydetected normalized light sensitivity of the macula lutea, no relativescotoma on the nasal side in OS, whereas an absolute scotoma along thevertical meridian persisted. The data of electrophysiologicalexaminations within norm.

EXAMPLE 12

Female patient was given the diagnosis of partial atrophy of the opticnerves secondary to arachnoiditis sustained ten years before (at thepresent time the patient is 18 years old).

Visual acuity: OD--0.08, OS--0.1, unamenable to correction.

Ocular fundus in both eyes: the optic disk pallid, borders clear-cut,vascular bed correct.

Fields of colour vision: red--narrowed, blue and green--notdiscriminated. Computerized perimetry revealed multiple paracentralscotomata in both eyes, largely in the area of projection of thepapillomacular bundle.

The patient was subjected to 10 4-minute sessions of magneticstimulation with a magnetic field having an induction of 0.25 T.Computerized perimetry revealed persisted relative scotomata in thecentre and paracentrally in the zone of projection of the papillomacularbundle.

The proposed method for treatment of diseases of the optic tract and thedevice for carrying said method into effect are contraindicated in thefollowing diseases and under the following conditions:

1. Neoplasms in the area to be exposed to the magnetic effect.

2. Retinal detachment.

3. Purulent iridocyclitis, endophthalmitis, panophthalmitis.

4. Metallic foreign bodies in the eyeball.

5. High intraocular pressure.

6. Pronounced vascularization of the corneal scar.

Practical application of the proposed method for treatment of diseasesof the optic tract and of the device for carrying said method intoeffect are instrumental in:

1. Enhancing visual functions 2 to 15 times as for visual acuity,depending on etiology of the disease, restoring colour perception whenthe latter has been absent beforehand, reducing the area of scotomataand increasing the visual angle threefold.

2. Attaining higher efficacy of treatment in late results up to one yearwhenever no favourable results have been obtained with other treatmentmethods (laser-assisted, pharmacological, reconstructive vasoplasty,acupuncture, and electropuncture).

3. Cutting the treatment period down to 15 days, i.e., to one course,consisting of 15 magnetic therapy sessions.

What is claimed is:
 1. A method for the treatment of diseases of theoptic tract, comprising applying a rotating magnetic field at a variableangular velocity synchronized with the pulse rate of the internalcarotid artery in any sequence to the bridge of the nose, to the upperportion of the orbit of both eyes with the eyelids closed, to thetemporal areas close to the external orbital margin of both eyes, toboth of the auriculo-temporal regions at the level of a projection ofthe optic decussation, and to the region of a projection of the visualanalyzers on the occipital protuberances.
 2. The method of claim 1wherein the rotating magnetic field has a maximum induction of from 0.1to 0.25 T.
 3. The method of claim 1 comprising applying said rotatingmagnetic field to each of said areas for from 1 to 5 minutes.
 4. Themethod of claim 2 comprising applying said rotating magnetic field toeach of said areas for from 1 to 5 minutes.